Psoriasis is an inflammatory and proliferative disease of the skin. Some evidences indicate that psoriasis is a T-cell mediating autoimmune disease although the pathogenesis is still unclear. To study the onset mechanisms of psoriasis, here we have established transgenic mice.Various cytokines may orchestrate the pathogenesis by controlling the interaction between T cells and keratinoctes. Among them, cytokines of IL6 family activate stat3 pathway. We have provided stat 3 conditional knock out mice (K5-Cre : Stat3^<flox/->) that loose stat 3 in keratinocytes by way of the cre-loxP strategy. These mutant mice have expressed spontaneous ulcers. This phenotype was not due to supressed proliferation but to impaired migration of keratinocytes.Antigens expressed in keratinocytes are presumably targets for the autoimmune response of T cells. Based on this idea, we have established transgenic mice expressing chicken ovalbumin (OVA) as a model antigen under keratin-5 promoter (K5-mOVA). MHC class II promoter-mOVA transgenic (II-mOVA) mice were used as a control. From the experiment with transfer of OVA specific T cells (OT-I) into K5-mOVA, antigens expressed in the epidermis are constitutively presented to T cells in the draining lymph nodes. T cells recognized the antigen, followed by proliferation tha was detected with the CFSE method. T cells carryng green fluorescence protein (GFP) started infiltrating the skin on day 5 after transfer. This migration induced non-specific infiltration of host T cells and acanthosis as well. Some of OVA-specific TCR and K5-mOVA double transgenic mice showed inflammation of the skin and scaling although the incidence was around 5 percent. Now we are providing athymic (nude) K5-mOVA mice having been transplanted with TCR transgenic bone marrow, followed by transplantation with normal irradiated thymus to see whether T cells currently generated from the thymus induce skin diseas or not.